Cardiovascular disease (CVD) is the leading cause of death in the United States, however, the classic risk factors do not explain all of its clinical and epidemiological features (Leaverton et al., J. Chronic. Dis. 40:775-784 (1987)). An increasing body of evidence suggests that bacterial infections also play a role. Low-grade infections have been associated with CVD and studies indicate that chronic infections, including those of the oral cavity, increase the risk of CVD. (Haverkate et al., Lancet 349: 462-466 (1997); Mattila et al., Clin. Infect. Dis. 26:719-734 (1998); Beck et al., J. Periodontol. 67:1123-1137 (1996)). It has been proposed that some risk factors are shared by periodontal disease and heart disease indicating a possible common etiologic pathway.
In a recent report, Haraszthy et al., (J. Periodontol. 71:1554-1560 (2000)) suggested that certain species of periodontal pathogenic bacteria may be involved in CVD. Additionally, Porphyromonas gingivalis, Prevotella intermedia, Actinobacillus actinomycetemcomitans and Bacteroides forsythus were detected within atheromatous plaques. P. gingivalis (Pg) is one of the major pathogens associated with adult periodontitis (Socransky et al., J. Periodontol. 63:322-331 (1992)) and, due to transient bacteremias, have a route to the circulatory system in periodontitis patients (Sconyers et al., J. Am. Dent. Assoc. 87:616-622 (1973); Silver et al., (J. Clin. Periodontol. 4:92-99 (1977)). Some studies have demonstrated that Pg internalizes within gingival epithelial cells in vitro and in vivo as well as within coronary endothelial cells in vitro (Lamont et al., Oral Microbiol. Immunol. 7:364-367 (1992); Sandros et al., J. Periodontal Res. 28:19-226 (1993); Rudney et al., Infect. Immun. 69:2700-2707 (2001); Deshpande et al., Infect. Immum. 66:5337-5343 (1998); Dorn et al., Infect. Immun. 67:5792-5798 (1999)). Thus, the inflammatory response of atherosclerosis may be a result of invasion by Pg within endothelial cells. Identification of polynucleotides and polypeptides in the invasive mechanism of Pg is needed. Mutational analyses are currently in progress to understand the role of genes in invasion ability of Pg. The knowledge of the role of these genes may offer insight into disease mechanisms and the interactions between bacteria and host. Thus, potential therapeutic interventions may be developed.